title: Role of the aryl hydrocarbon receptor in the pathogenesis of chronic rhinosinusitis with nasal polyps.
abstract: A predominant Th17 population is a marker of chronic rhinosinusitis with nasal polyps (CRSwNP) in Chinese patients. As a ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR) plays a vital role in promoting or inhibiting specific Th cell development. However, its role in CRSwNP remains to be defined. The aim of the present study was to investigate whether AhR, which regulates Th17 cell differentiation, played a role in the pathogenesis of CRSwNP by evaluating AhR expression in nasal polyps and peripheral blood mononuclear cells (PBMCs) obtained from CRSwNP patients. Forty-eight patients (atopic, 24; non-atopic, 24) and 13 controls were studied. To explore the role of AhR in CRSwNP, we analyzed the expression of AhR, retinoid-related orphan receptor C (RORC), interleukin (IL)-17, and IL-10 and the differentiation of Th17 using mRNA or protein detection methods. Notably, the expression of AhR was reduced in CRSwNP, and the expression of AhR was lower in the atopic group than in the non-atopic group. However, there was a very low level of Th17 and its associated factors (RORC, IL-17) in the control group compared to the two CRSwNP groups. In particular, the polarization of Th17 cells in atopic CRSwNP patients was increased compared with non-atopic individuals. In addition, ITE intervention in PBMCs promoted AhR expression and attenuated Th17 responses, demonstrating that AhR was more likely to suppress Th17 cells differentiation in Chinese CRSwNP patients. This information is valuable for obtaining a clear understanding of the pathogenesis of CRSwNP. Moreover, patients with atopic CRSwNP may exhibit reduced expression of AhR, leading to aggravation of the disproportionate distribution of Th17 cells in polyp tissues and PBMCs, thereby suggesting that atopic CRSwNP has a distinct pathogenesis from that of non-atopic CRSwNP.
authors.affiliation: Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Yixueyuan Road 1#, Chongqing, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Wei
authors.forename: Guo-Hua
authors.initials: GH
authors.lastname: Hu
authors.forename: Hou-Yong
authors.initials: HY
authors.lastname: Kang
authors.forename: Hong-Bing
authors.initials: HB
authors.lastname: Yao
authors.forename: Wei
authors.initials: W
authors.lastname: Kou
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhang
authors.forename: Su-Ling
authors.initials: SL
authors.lastname: Hong
mesh_terms: D000328:Adult; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics / Q000378:metabolism*; D016022:Case-Control Studies; D002454:Cell Differentiation; D002478:Cells, Cultured; D002681:China; D002908:Chronic Disease; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics / Q000378:metabolism*; D012220:Rhinitis / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction; D012852:Sinusitis / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism*; D055815:Young Adult
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D016753:Interleukin-10; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D018336:Receptors, Aryl Hydrocarbon; C111235:AHR protein, human; C508609:IL10 protein, human; C539900:RORC protein, human